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Ovary & Fallopian Tube

C56-C57WHO Vol. 4
Female Reproductive System

Prognosis

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🔬 Histological Types

📚 Latest Research

2026-09-10

Trigonelline reverses cisplatin resistance in ovarian cancer cells by modulating ferroptosis via the Nrf2/GPX4 pathway.

Li J, et al

Trigonelline, a natural plant alkaloid, reverses cisplatin (DDP) resistance in ovarian cancer by promoting ferroptosis — an iron-dependent form of programmed cell death — through suppression of the Nrf2/GPX4 signaling pathway. Using DDP-resistant ovarian cancer cell lines SKOV-3/DDP and A2780/DDP, researchers demonstrated that combining low, non-toxic concentrations of trigonelline with DDP induced greater mitochondrial damage than DDP alone, increasing reactive oxygen species (ROS), lipid peroxidation, malondialdehyde (MDA), and Fe²⁺ levels while reducing superoxide dismutase (SOD) activity and the GSH/GSSG ratio. The combined treatment also downregulated key ferroptosis-resistance proteins Nrf2, HO-1, GPX4, and SLC7A11, and critically, overexpression of Nrf2 fully reversed these effects, confirming the pathway's central role. These findings position trigonelline as a promising natural compound for overcoming platinum resistance in ovarian cancer, warranting further preclinical and clinical investigation.

Toxicon : official journal of the International Society on Toxinology

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2026-09-09

Bacteria-Based Ammunition for Cascade-Amplified Chemoimmunotherapy of Ovarian Cancer.

Miao Z, et al

Researchers developed a dual-responsive bacterial-nanoparticle system called VNP@BD-Poly — combining attenuated Salmonella VNP20009 with a BSA-doxorubicin polymer complex — that targets the hypoxic, immunosuppressive tumor microenvironment of ovarian cancer and releases doxorubicin in a pH/GSH-responsive manner to trigger immunogenic cell death. The system exploits a "bacterial sensitization–DOX antigen release–immune cascade" loop to activate antitumor immunity, reverse immunosuppression, and suppress tumor progression with minimal systemic toxicity. This preclinical study offers a promising and versatile chemoimmunotherapy platform with potential translational value for ovarian cancer and other solid tumors.

Nano letters

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2026-09-08

PARP16 is a Druggable Regulator of Ribosome MARylation and Protein Homeostasis in Ovarian Cancer Cells.

Challa S, et al

A new study establishes PARP16 as a pharmacologically tractable target in ovarian cancer, showing that the selective small-molecule inhibitor DB008 disrupts ribosomal mono(ADP-ribosyl)ation (MARylation), impairs protein homeostasis, and significantly inhibits tumor growth in OVCAR3 xenograft models. DB008 reduced PARP16 auto-MARylation and ribosome-associated MARylation in ovarian cancer cells, enhanced global protein synthesis, increased protein aggregation, and suppressed both cell proliferation and anchorage-independent colony formation. CRISPR-mediated deletion of PARP16 abolished all cellular effects of DB008, and expression of a DB008-resistant PARP16 mutant confirmed strict on-target activity, ruling out off-target contributions. These findings provide pharmacologic proof-of-concept that disrupting the NAD⁺–PARP16–ribosome axis is a viable therapeutic strategy for ovarian cancer.

The Journal of biological chemistry

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💊 Therapies

Surgery
Chemotherapy
Targeted therapies

🥗 Diet

Excess body fatness and cancer risk

🫙 Supplements

High-dose vitamin C (including intravenous infusions) Alpha-lipoic acid and chemotherapy-induced peripheral neuropathy

🧪 Tumor markers

Cancer antigen 125 Human epididymis protein 4 Alpha-fetoprotein

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